and HBeAg(-) patients - World Journal of Gastroenterology

More documents

Recommendations

Info

Online Submissions: http://www.wjgnet.com/1007-9327office wjg@wjgnet.com doi:10.3748/wjg.v17.i6.735 Non-alcoholic fatty liver disease: An early mediator predicting metabolic syndrome in obese children? Jun-Fen Fu, Hong-Bo Shi, Li-Rui Liu, Ping Jiang, Li Liang, Chun-Lin Wang, Xi-Yong Liu Jun-Fen Fu, Hong-Bo Shi, Li-Rui Liu, Ping Jiang, Li Liang, Chun-Lin Wang, Department of Endocrinology, The Children’s Hospital of Zhejiang University School of Medicine, Hangzhou 310003, Zhejiang Province, China Hong-Bo Shi, Department of Pediatrics, Yinzhou People’s Hospital, Ningbo 315400, Zhejiang Province, China Ping Jiang, The First People’s Hospital of Hangzhou, Hangzhou 310003, Zhejiang Province, China Xi-Yong Liu, Clinical and Molecular Pharmacology, City of Hope National Medical Center, Duarte, CA 91009, United States Author contributions: Fu JF, Shi HB, Liu LR and Jiang P substantially contributed to the conception and design of the study; Fu JF and Shi HB also wrote the manuscript; Wang CL collected and input the data; Liang L interpreted the data; Liu XY performed statistical analysis. Supported by Zhejiang Provincial Natural Science Foundation, No. Y2080047; funds for Zhejiang Major Medical and Health Science and Technology Program and funds from Ministry of Health, No. WKJ2008-2-026; Major Special Zhejiang Provincial Science and Technology Fund, No. 2008c03002-1; and the National Key Technology R&D Program of China, No. 2009BAI80B01 Correspondence to: Jun-Fen Fu, MD, PhD, Department of Endocrinology, The Children’s Hospital of Zhejiang University School of Medicine, 57 Zhugan Avenue, Hangzhou 310003, China. fjf68@yahoo.com.cn Telephone: +86-571-87061007 Fax: +86-571-87033296 Received: July 20, 2010 Revised: September 6, 2010 Accepted: September 13, 2010 Published online: February 14, 2011 Abstract AIM: To investigate if non-alcoholic fatty liver disease (NAFLD) is an early mediator for prediction of metabolic syndrome, and if liver B-ultrasound can be used for its diagnosis. METHODS: We classified 861 obese children (6-16 years old) into three subgroups: group 0 (normal liver in ultrasound and normal transaminases); group 1 (fatty liver in ultrasound and normal transaminases); and group 2 (fatty liver in ultrasound and elevated transaminases). WJG|www.wjgnet.com World J Gastroenterol 2011 February 14; 17(6): 735-742 ISSN 1007-9327 (print) ISSN 2219-2840 (online) © 2011 Baishideng. All rights reserved. We measured the body mass index, waist and hip circumference, blood pressure, fasting blood glucose, insulin, homeostasis model assessment of insulin resistance (HOMA-IR), whole-body insulin sensitivity index (WBISI), lipid profile and transaminases in all the participants. The risk of developing metabolic syndrome (MS) was assessed according to the degree of liver fatty infiltration based on the B-ultrasound examination. RESULTS: Among the 861 obese children, 587 (68.18%) were classified as having NAFLD, and 221 (25.67%) as having MS. The prevalence of MS in NAFLD children (groups 1 and 2) was 37.64% (221/587), which was much higher than that in non-NAFLD group (group 0, 12.04%) (P < 0.01). There were significantly higher incidences concerning every component of MS in group 2 compared with group 0 (P < 0.05). The incidence of NAFLD in MS patients was 84.61% (187/221), which was significantly higher than that of hypertension (57.46%, 127/221) and glucose metabolic anomalies (22.62%, 50/221), and almost equal to the prevalence of dyslipidemia (89.14%, 197/221). Based on the B-ultrasound scales, the presence of moderate and severe liver fatty infiltration carried a high risk of hypertension [odds ratio (OR): 2.18, 95% confidence interval (95% CI): 1.27-3.75], dyslipidemia (OR: 7.99, 95% CI: 4.34-14.73), impaired fasting glucose (OR: 3.65, 95% CI: 1.04-12.85), and whole MS (OR: 3.77; 95% CI: 1.90-7.47, P < 0.01). The state of insulin resistance (calculated by HOMA-IR and WBISI) deteriorated as the degree of fatty infiltration increased. CONCLUSION: NAFLD is not only a liver disease, but also an early mediator that reflects metabolic disorder, and liver B-ultrasound can be a useful tool for MS screening. © 2011 Baishideng. All rights reserved. ORIGINAL ARTICLE Key words: Childhood obesity; Non-alcoholic fatty liver disease; Metabolic syndrome; Liver B ultrasonography 735 February 14, 2011|Volume 17|Issue 6|
Fu JF et al . NAFLD and metabolic syndrome Peer reviewer: Michael L Schilsky, MD, Associate Professor of Medicine and Surgery, Yale University School of Medicine, 333 Cedar Street, LMP 1080, New Haven, CT 06520, United States Fu JF, Shi HB, Liu LR, Jiang P, Liang L, Wang CL, Liu XY. Non-alcoholic fatty liver disease: An early mediator predicting metabolic syndrome in obese children? World J Gastroenterol 2011; 17(6): 735-742 Available from: URL: http://www.wjgnet.com/1007-9327/full/v17/i6/735.htm DOI: http://dx.doi. org/10.3748/wjg.v17.i6.735 INTRODUCTION There is a growing concern for non-alcoholic fatty liver disease (NAFLD) and metabolic syndrome (MS) in obese children [1-3] . NAFLD is a clinicopathological syndrome that ranges from simple steatosis to steatohepatitis, fibrosis or cirrhosis of the liver [4] . It is associated with dyslipidemia, obesity, and insulin resistance, which are the main features of MS. NAFLD and MS often are seen in the same individual [5-8] , whereas insulin resistance probably is a key event that links them together. The mortality of patients with NAFLD has increased significantly among the general population, and cardiovascular risk competes with liverrelated risk in dictating the final outcome [9,10] . Several prospective studies in adults have demonstrated that NAFLD is associated with an increased incidence of MS and type 2 diabetes mellitus in elderly patients, and independent patients with obesity [11-14] . Thus, NAFLD may be not only a liver disease, but also an early mediator of type 2 diabetes mellitus and MS in adults. However, the impact of NAFLD on MS among the young population is still not clear. The debate remains as to whether NAFLD should be included as one of the components of the MS. This study aimed to assess idiopathic NAFLD among Chinese obese children, to verify the prevalence of MS in NAFLD patients based on B-ultrasound scan, and to investigate whether NAFLD is associated with MS and MS profile, and whether it is an important risk factor for MS as well. MATERIALS AND METHODS Study design and population A total of 861 obese children and adolescents, aged between 6 and 16 years, who were referred to our endocrinology department with the complaint of obesity from January 2004 to September 2009, were enrolled in this study. Based on an accepted criteria for obesity diagnosis in Chinese children [15] , all the participants had a body mass index (BMI) that was above the 95th percentile for their age and sex, based on the national reference data in 2004 [16] . Exclusion criteria were the known presence of endocrine metabolic or kidney diseases, and the use of medication that altered blood pressure, liver function, and glucose or lipid metabolism. The demographic distribution of subjects is displayed in Table 1. Participants underwent a routine clinical examination, including physical examination, biochemical tests, oral glucose tolerance WJG|www.wjgnet.com Table 1 Characteristics of 861 obese patients Girls (n = 263) Boys (n = 598) Age (yr) 10.53 ± 2.26 10.81 ± 1.97 Tanner stage (T1/T2-4) 126/137 287/311 BMI (kg/m 2 ) a 27.68 ± 4.24 28.38 ± 3.47 BMI Z-score a 4.31 ± 1.58 3.05 ± 1.16 WHR (waist/hip ratio) a 0.93 ± 0.07 0.96 ± 0.05 Waist (cm) a 86.53 ± 11.83 90.91 ± 10.25 Systolic pressure (mmHg) a 114.47 ± 13.50 117.33 ± 12.55 Diastolic pressure (mmHg) 67.85 ± 9.32 68.99 ± 9.00 Cholesterol (mmol/L) 4.48 ± 1.01 4.43 ± 0.93 Triglycerides (mmol/L) 1.79 (0.19-5.17) 1.77 (0.17-10.78) HDL 1.23 ± 0.28 1.26 ± 0.34 LDL a 2.69 ± 0.73 2.51 ± 0.68 AI a 2.30 ± 0.83 2.11 ± 0.74 Uric acid (μmol/L) 377.0 (203.2-705.4) 383.0 (198.2-708.5) Fasting glucose (mmol/L) 4.87 ± 0.58 4.90 ± 0.57 120-min glucose (mmol/L) a 6.31 ± 1.52 6.01 ± 1.44 HbA1c (%) 5.74 ± 0.57 5.69 ± 0.52 Fasting insulin (mIU/L) a 17.9 (0.3-303.0) 15.3 (0.3-219.0) HOMA-IR a 3.77 (0.07-78.11) 3.33 (0.07-51.59) WBISI a 2.59 (0.39-11.90) 3.37 (0.52-24.19) ALT (U/L) a 37.5 (8.0-283.0) 29.0 (4.0-561.0) a P < 0.05 boys vs girls. Data are expressed as mean ± SD or median (range). BMI: Body mass index; HDL: High-density lipoprotein; LDL: Low-density lipoprotein; AI: Atherogenic index; HOMA-IR: Homeostasis model assessment of insulin resistance; WBISI: Whole-body insulin sensitivity index; ALT: Alanine aminotransferase. test (OGTT) and liver ultrasonographic scanning. There was no difference in age and Tanner stages between boys and girls. However, significant differences existed in clinical, anthropometric and laboratory data in relation to sex (Table 1). The protocol was approved by the Medical Ethics Committee of The Children’s Hospital of Zhejiang University School of Medicine. Written informed consent from parents (or guardians) and children (where appropriate) were obtained. Definition of disease, syndrome and disorders NAFLD: NAFLD was defined according to the revised definition and treatment guidelines for NAFLD by the Chinese Hepatology Association in February 2006 [17] , and was diagnosed by means of a protocol using clinical, laboratory and ultrasound examinations in combination. In this study, NAFLD was diagnosed as a diffusely echogenic change on liver B-ultrasonography (fatty infiltration in liver), with or without elevated serum aminotransferase levels and other factors that can cause liver fatty infiltration or aminotransferase elevation, such as hepatitis virus infection, drug-induced injury, and other metabolic diseases, such as Wilson’s disease, were excluded. There was no history of current or past alcohol drinking. Two subgroups were classified in NAFLD obese children: group 1 (fatty liver in ultrasound and normal transaminases) and group 2 (fatty liver in ultrasound and elevated transaminases). Group 0 was diagnosed as obese children without liver disorder (normal liver in ultrasound and normal transaminases). 736 February 14, 2011|Volume 17|Issue 6|
Page 1 and 2:
World Journal of Gastroenterology W
Page 3 and 4:
Robert JL Fraser, Daw Park Jacob Ge
Page 5 and 6:
Italy Donato F Altomare, Bari Piero
Page 7 and 8:
Fernando Azpiroz, Barcelona Ramon B
Page 9 and 10:
S Contents EDITORIAL REVIEW ORIGINA
Page 11 and 12:
Contents ACKNOWLEDGMENTS APPENDIX A
Page 13 and 14:
Jahn KA et al . Colon cancer and li
Page 19 and 20: Jahn KA et al . Colon cancer and li
Page 21 and 22: Jahn KA et al . Colon cancer and li
Page 23 and 24: Săftoiu A. Imaging techniques in E
Page 29 and 30: Ghimire P et al . Primary GI lympho
Page 33: Ghimire P et al . Primary GI lympho
Page 39: Online Submissions: http://www.wjgn
Page 42 and 43: Table 2 Comparison of hepatitis B e
Page 45 and 46: Utama A et al . HBV core promoter m
Page 47 and 48: Utama A et al . HBV core promoter m
Page 49 and 50: Motoki T et al . Glutamine depletio
Page 51 and 52: Table 2 Nutrient composition of mou
Page 53 and 54: A Motoki T et al . Glutamine deplet
Page 55 and 56: A Counts B % of sub-G0 cell populat
Page 57 and 58: Motoki T et al . Glutamine depletio
Page 59 and 60: Hu JD et al . Urinary metabolomic p
Page 61 and 62: Abundance/× 10 6 Abundance/× 10 6
Page 63 and 64: A Regression factor scores 2 for an
Page 65: Hu JD et al . Urinary metabolomic p
Page 70 and 71: developing hypertension (OR: 2.18,
Page 72 and 73: obese and exhibited higher insulin
Page 74 and 75: Online Submissions: http://www.wjgn
Page 77 and 78: Roberts SE et al . Perinatal factor
Page 79 and 80: Roberts SE et al . Perinatal factor
Page 83 and 84: Oksaharju A et al . Probiotics regu
Page 91: Online Submissions: http://www.wjgn
Page 96 and 97: Factors associated with improved su
Page 101 and 102: Koehler-Santos P et al . Identifica
Page 103 and 104: Koehler-Santos P et al . Identifica
Page 109: Goenka MK et al . Capsule endoscopy
Page 113 and 114: Tatsuki M et al . Hypermagnesemia a
Page 117 and 118:
Chang CC et al . Parity and gastric
Page 119 and 120:
Chang CC et al . Parity and gastric
Page 121 and 122:
Zhang XQ et al . EEA model of guine
Page 123 and 124:
Table 3 Measurement of common bile
Page 125 and 126:
Zhang XQ et al . EEA model of guine
Page 127 and 128:
Online Submissions: http://www.wjgn
Page 129:
Zhao R et al . Gene expression anal
Page 133 and 134:
Zhao R et al . Gene expression anal
Page 135 and 136:
Page 137 and 138:
Qiu HB et al . HBV infection and li
Page 139 and 140:
Qiu HB et al . HBV infection and li
Page 141:
Shen H et al . K-ras and BRAF mutat
Page 145 and 146:
Page 147 and 148:
Page 149 and 150:
Page 151 and 152:
Instructions to authors Indexed and
Page 153 and 154:
Instructions to authors uniform leg
Page 155:
Instructions to authors Language ev
show all

and HBeAg(-) patients - World Journal of Gastroenterology

You also want an ePaper? Increase the reach of your titles

Delete template?

Save as template?